DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant’s election without traverse of Group I, claims 1-5, 7-11, and 13-14, in the reply filed on 10/7/2025 is acknowledged.
Claims 15-16, 18-19, 22, and 24-27 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 10/7/2025.
Claims 1-5, 7-11, & 13-14 are under examination on the merits.
Information Disclosure Statement
The Information Disclosure Statements (IDSs) submitted on 9/13/2022, 10/7/2022, 4/24/2024, 6/11/2024, and 10/01/2024 are in compliance with 37 CFR 1.97. Accordingly, the IDSs are being considered by the examiner.
Specification
The disclosure is objected to because of the following informalities: the “BRIEF DESCRIPTION OF THE DRAWINGS” section makes multiple references to colors (Fig. 1, “red”, “blue”), but no petition for the use of colored drawings has been granted.
The “FIGS. 1A-1E” description also references “FIG. 9A”, “FIG. 9B”, “FIG. 9C”, “FIG. 9D”, and “FIG. 9E, which appear to be typographical mistakes.
Appropriate correction is required.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1, 3, 7, 10-11, & 13-14 are rejected under 35 U.S.C. 103 as being unpatentable over Kirn et al. (PGPub US 20190255192 A1, filed 11/9/2018, published 8/22/2019; hereinafter referred to as “Kirn”) in further view of Miller et al. (PGPub US 20100273256 A1, filed 4/8/2009, published 10/28/2010; hereinafter referred to as “Miller”), Nenoi et al. (PGPub US 20080019946 A1, filed 4/19/2007, published 1/24/2008; hereinafter referred to as “Nenoi”) and Mallet et al. (PGPub US 20060051331 A1, filed 4/29/2003, published 3/9/2006; hereinafter referred to as “Mallet”).
The claimed invention encompasses an adeno-associated viral (AAV) gene therapy vector comprising: a 5’ inverted terminal repeat (ITR) comprising SEQ ID NO: 23, a retinal pigment epithelium (RPE) specific promoter, a polynucleotide that encodes a Kir7.1 protein and has at least 90% identity to SEQ ID NO: 25, a posttranscriptional regulatory element (PRE), a polyadenylation signal, and a 3’ ITR of SEQ ID NO: 28 (claim 1). In a specific embodiment, the posttranscriptional regulatory element is a woodchuck PRE comprising SEQ ID NO: 26 (claim 3). In another embodiment, the claimed invention encompasses a construct comprising the AAV gene therapy vector (claim 7). A different embodiment is a therapeutic composition comprising the AAV gene therapy vector and a pharmaceutically acceptable carrier (claim 14).
The claimed invention also encompasses a cell comprising the construct, wherein the cell is capable of producing AAV virus particles comprising the AAV gene therapy vector and is capable of expressing the Kir7.1 protein (claim 10), and the cell further comprises helper plasmids that encode AAV proteins required to produce AAV virus particles (claim 11). Another embodiment of the claimed invention is an AAV virus particle made by the cell (claim 13).
The Prior Art
Kirn teaches AAV vectors that comprise transgenes (heterologous polynucleotides) for gene therapy (paras. [0010], [0054], [0088], and [00247-0048]), wherein the heterologous polynucleotide is flanked by AAV ITRs (para. [0054]), & [0088]). Kirn further discloses that the AAV may comprise an RPE specific promoter linked to the transgene, which can be a KCNJ13 gene, which encodes Kir7.1 protein (paras. [0224] & [0217]). Additionally, Kirn’s compositions encompass rAAV virions (viral particles), which include an rAAV polynucleotides, as well as polynucleotides encoding rAAV, such as plasmids (para. [0053]). Kirn also discloses host cells useful for producing rAAV, which can be stably genetically modified with a nucleic acid or transiently genetically modified with a nucleic acid (para. [0231]). Furthermore, Kirn teaches that helper virus functions, which allow AAV replication and packaging, may be provided in a number of ways, including by providing helper virus or polynucleotide sequences encoding the requisite functions to a producer cell in trans, by a plasmid or other expression vector (para. [0057]). Kirn also provides a pharmaceutical composition comprising rAAV and a pharmaceutically acceptable carrier, diluent, excipient, or buffer suitable for use in a human or non-human patient (para. [0232]). Notably, Kirn fails to specifically teach i) the vector comprising a PRE, ii) the vector comprising a polyadenylation signal, iii) the 5’ ITR comprising SEQ ID NO: 23, iv) the 3’ ITR comprising SEQ ID NO: 28, or v) the polynucleotide encoding Kir7.1 having at least 90% sequence identity to SEQ ID NO: 25. However, an AAV vector with those limitations would have been obvious to one of ordinary skill in the art in view of Miller and Nenoi.
Miller teaches viral vectors comprising a KCNJ13 gene that is 99% identical in sequence to SEQ ID NO: 25 (see Appendix A: alignment of the instant SEQ ID NO: 25 with Miller’s SEQ ID NO: 1; Miller, Table 1, Abstract, generally, paras. [0022], [0057], [0091]). Miller further teaches that its compositions may be used for modulation of the gene activity in vivo for prophylactic and therapeutic purposes (Abstract).
Nenoi teaches AAV gene therapy vectors comprising a 5’ ITR that is 100% identical in sequence to SEQ ID NO: 23, a therapeutic gene sequence, a polyadenylation sequence, and a 3’ ITR that is 100% identical in sequence to SEQ ID NO: 28 (paras. [0009] & [0039-0041]; 5’ ITR and 3’ITR sequences labeled as “SEQ ID NO: 4” and “SEQ ID NO: 5” in Nenoi, respectively).
Mallet teaches vectors, compositions, and methods for delivering transgenes into mammalian cells (Abstract). Mallet further discloses that of various tested elements and sequences from eukaryotic mRNAs that could enhance transgene expression in mammalian cells, WPRE gave the highest level of expression (paras. [0022-0026]). Additionally, Mallet discloses the WPRE element sequence, SEQ ID NO: 1, which from nucleotides 7-604 is 100% identical to the instant SEQ ID NO: 26 (Mallet SEQ ID NO: 1). Mallet further discloses that the vectors may be plasmids, recombinant viruses, or specifically AAVs (para. [0038]). Further, Mallet discloses that its compositions and methods may be used in epithelial cells and other tissues, organs, or cell types (para. [0048]).
It would have been obvious to one of ordinary skill in the art to modify the AAV construct taught by Kirn to incorporate the KCNJ13 gene encoding Kir7.1 taught by Miller, ITRs and polyadenylation sequence taught by Nenoi, and WPRE taught by Mallet. One of ordinary skill in the art would have been motivated to generate an AAV vector that expresses the KCNJ13 gene in target cells. Therefore, claims 1, 3, 7, 10-11, & 13-14 were prima facie obvious before the priority date of the instant invention.
Claim 2 is rejected under 35 U.S.C. 103 as being unpatentable over Kirn, Miller, Nenoi, and Mallet (supra) as applied to claims 1, 3, 7, 10-11, & 13-14 above, and further in view of Petrukhin et al. PGPub US 20060105364 A1, filed 9/27/2005, published 5/18/2006; hereinafter referred to as “Petrukhin”).
In a specific embodiment, the RPE specific promoter is a VMD2 promoter comprising a polynucleotide having at least 90% sequence identity to SEQ ID NO: 24 (claim 2).
The Prior Art
The teachings of Kirn, Miller, Nenoi, and Mallet are described above. However, they do not teach that the RPE specific promoter is a VMD2 promoter comprising a polynucleotide having at least 90% sequence identity to SEQ ID NO: 24.
Petrukhin teaches human and mouse DNA sequences that encode the gene CG1CE, which, when mutated, is responsible for Best’s macular dystrophy (Abstract). Petrukhin further discloses that Best’s macular dystrophy is also known as hereditary macular dystrophy or Best’s vitelliform macular dystrophy (VMD2; para. [0005]). Petrukhin also discloses a human genomic CG1CE DNA that has the nucleotide sequence SEQ ID NO: 1, which is localized to the RPE, which has a fragment with 100% sequence identity to the instant SEQ ID NO: 24 (nts 4582-5557, paras. [0020,0119-0120]).
It would have been obvious to one of ordinary skill in the art to modify the teachings of Kirn, Miller, Nenoi, and Mallet to incorporate the VMD2 promoter taught by Petrukhin. Kirn teaches that in some instances, a nucleotide sequence encoding a gene product of interest is operably linked to a RPE cell-specific promoter, and that VMD2 promoter is a suitable RPE-specific regulatory element (p. 32, col. 2, para. 1). Petrukhin teaches a VMD2 nucleotide sequence with a domain that is 100% identical to SEQ ID NO: 24. One of ordinary skill in the art would have been motivated to express Kir7.1 in RPE under a promoter known to be active in the RPE. There would have been a reasonable expectation of success because the components of the vector were known and shown to be functional in the prior art. Therefore, claim 2 was prima facie obvious before the priority date of the instant invention.
Claim 4 is rejected under 35 U.S.C. 103 as being unpatentable over Kirn, Miller, Nenoi, and Mallet (supra) as applied to claims 1, 3, 7, 10-11, & 13-14 above, and further in view of Wang, et al. (Gene Therapy 1999, 6: 667-675 doi: 10.1038/sj.gt.3300856. PMID: 10476227; hereinafter referred to as “Wang”) as evidenced by GenBank accession: MG550105.1 (1/10/2018).
In a specific embodiment, the polyadenylation signal comprises SEQ ID NO: 27 (claim 4).
The Prior Art
The teachings of Kirn, Miller, Nenoi, and Mallet are described above. However, they do not teach that the polyadenylation signal comprises SEQ ID NO: 27.
Wang teaches AAV-based gene therapy vectors (Abstract), that can accommodate a transcriptional cassette including promoter and polyadenylation signal (p. 668, col. 1, para. 3). Wang further discloses that Bovine growth hormone (BGH) polyadenylation signal was the strongest of various polyadenylation signals tested (Fig. 2). GenBank accession: MG550105.1 (1/10/2018) provides evidence that the nucleotide sequence of BGH is 100% identical to SEQ ID NO: 27.
It would have been obvious to one of ordinary skill in the art to modify the teachings of Kirn, Miller, Nenoi, and Mallet to incorporate the BGH polyadenylation signal taught by Wang as evidenced by GenBank accession: MG550105.1. Kirn discloses that its vectors may comprise a polyadenylation signal, and Wang teaches that BGH polyadenylation signal is the strongest, and is applicable for AAV vectors for mammalian expression. One of ordinary skill in the art would have been motivated to express Kir7.1 efficiently. There would have been a reasonable expectation of success because the components of the vector were known and shown to be functional in the prior art. Therefore, claim 4 was prima facie obvious before the priority date of the instant invention.
Claim 8 is rejected under 35 U.S.C. 103 as being unpatentable over Kirn, Miller, Nenoi, and Mallet (supra) as applied to claims 1, 3, 7, 10-11, & 13-14 above, and further in view of Miller et al. (J Virol. 2005 Sep;79(17):11434-42. doi: 10.1128/JVI.79.17.11434-11442.2005. PMID: 16103194; hereinafter referred to as “Miller II”).
In a specific embodiment, the claimed invention encompasses a construct comprising the AAV gene therapy vector that is a plasmid that comprises an antibiotic resistance gene and an origin of replication and is capable of propagation in bacteria (claim 8)
The Prior Art
The teachings of Kirn, Miller, Nenoi, and Mallet are described above. However, they do not teach a construct comprising the AAV gene therapy vector that is a plasmid that comprises an antibiotic resistance gene and an origin of replication and is capable of propagation in bacteria.
Miller II teaches AAV vectors for human gene therapy, wherein vectors include a selectable bacterial marker and replication origin, and specifically the AAV shuttle vector AAV2-TOA, which contains a bacterial replication origin and antibiotic resistance genes (p. 11436, col. 2; Abstract; p. 11439, para. 1). Miller II discloses that such plasmid DNAs from bacteria may be used for AAV vector production (p. 11435, para. 2).
It would have been obvious to one of ordinary skill in the art to modify the teachings of Kirn, Miller, Nenoi, and Mallet to incorporate a selectable bacterial marker and replication origin, as taught by Miller II. Miller II discloses that such plasmid DNAs can be purified from bacteria and used for vector production. One of ordinary skill in the art would have been motivated to use bacteria for AAV vector production. There would have been a reasonable expectation of success because the components of the vector were known and shown to be functional in the prior art. Therefore, claim 8 was prima facie obvious before the priority date of the instant invention.
Claim 5 is rejected under 35 U.S.C. 103 as being unpatentable over Kirn, Miller, Nenoi, Mallet, and Petrukhin (supra) as applied to claim 2 above, and further in view of Wang, et al. (supra) as evidenced by GenBank accession: MG550105.1 (1/10/2018).
In a specific embodiment, the vector comprises a polynucleotide having at least 90% sequence identity to SEQ ID NO: 31 (claim 5)
The Prior Art
The teachings of Kirn, Miller, Nenoi, Mallet, and Petrukhin are described above. However, they do not teach a vector that comprises a polynucleotide having at least 90% sequence identity to SEQ ID NO: 31.
Wang teaches AAV-based gene therapy vectors (Abstract), that can accommodate a transcriptional cassette including promoter and polyadenylation signal (p. 668, col. 1, para. 3). Wang further discloses that Bovine growth hormone (BGH) polyadenylation signal was the strongest of various polyadenylation signals tested (Fig. 2). GenBank accession: MG550105.1 (1/10/2018) provides evidence that the nucleotide sequence of BGH is 100% identical to SEQ ID NO: 27.
It would have been obvious to one of ordinary skill in the art to modify the teachings of Kirn, Miller, Nenoi, Mallet, and Petrukhin to incorporate the BGH polyadenylation signal taught by Wang as evidenced by GenBank accession: MG550105.1. Kirn discloses that its vectors may comprise a polyadenylation signal, and Wang teaches that BGH polyadenylation signal is the strongest, and is applicable for AAV vectors for mammalian expression. One of ordinary skill in the art would have been motivated to express Kir7.1 efficiently. Although the cited references do not specifically teach a vector comprising a polynucleotide having at least 90% identity to SEQ ID NO: 31, their combined components, which would have been obvious (as described in the present rejections), results in a vector having 95.8% identity to SEQ ID NO: 31 (5’ ITR + VMD2 promoter + KCNJ13 + WPRE + polyadenylation signal + 3’ ITR = 3147 nucleotides identical to SEQ ID NO: 31, which is 95.8% of SEQ ID NO: 31). There would have been a reasonable expectation of success because the components of the vector were known and shown to be functional in the prior art. Therefore, claim 5 was prima facie obvious before the priority date of the instant invention.
Claim 9 is rejected under 35 U.S.C. 103 as being unpatentable over Kirn, Miller, Nenoi, Mallet, and Petrukhin and Wang as evidenced by GenBank accession: MG550105.1 (supra) as applied to claim 5 above, and further in view of GenBank accession: MK801287.1 (5/18/2019).
The claimed invention encompasses a construct comprising a polynucleotide having at least 90% sequence identity to SEQ ID NO: 22 (claim 9).
The Prior Art
The teachings of Kirn, Miller, Nenoi, Mallet, Petrukhin, and Wang as evidenced by MG550105.1 are described above. However, they do not teach a construct comprising a polynucleotide having at least 90% sequence identity to SEQ ID NO: 22.
GenBank accession: MK801287.1 teaches an AAV cloning vector that possesses vector backbone, a replication origins, and an ampicillin resistance gene that is 99.8% identical (2592 of 2597 nucleotides) in sequence to the corresponding vector sequence features in SEQ ID NO: 22.
It would have been obvious to one of ordinary skill in the art to modify the teachings of Kirn, Miller, Nenoi, Mallet, and Petrukhin to incorporate AAV cloning vector backbone disclosed by GenBank: MK801287.1. As discussed above, though the cited references do not specifically teach a vector comprising a polynucleotide having at least 90% identity to SEQ ID NO: 31, their combined components, which would have been obvious (as described in the present rejections), results in a vector having 95.8% identity to SEQ ID NO: 31 (5’ ITR + VMD2 promoter + KCNJ13 + WPRE + polyadenylation signal + 3’ ITR = 3147 nucleotides identical to SEQ ID NO: 31, which is 95.8% of SEQ ID NO: 31). When the ITRs, promoter, Kir7.1-encoding sequence, WPRE, and polyadenylation sequences taught by Miller, Nenoi, Mallet, and Petrukhin are combined with the AAV cloning vector disclosed by MK801287.1, the resulting vector is 97.6% identical to the instant SEQ ID NO: 22 (5739 of 5880 nucleotides). One of ordinary skill in the art would have been motivated to generate an AAV cloning vector for Kir7.1 expression. There would have been a reasonable expectation of success because the components of the vector were known and shown to be functional in the prior art. Therefore, claim 9 was prima facie obvious before the priority date of the instant invention.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
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Claims 1-5, 7-11 and 13-14 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 6, 9-11, 13, 15-16, and 18-19 of copending Application No. 17/284,408 in view of Kirn, Miller, Nenoi, Mallet, Petrukhin, Miller II, Wang, as evidenced by GenBank accession: MG550105.1, and GenBank accession: MK801287.1 (supra). Although the claims are not identical, each set of claims encompasses a gene therapy vector comprising a VMD2 promoter and a polynucleotide encoding a Kir7.1 polypeptide (instant claims 1-2 and copending claims 1 & 6). Additionally, each set of claims encompasses the gene therapy vector being an AAV vector (instant claim 1, copending claims 10, 13, and 15). The differences in the applications are: i) the copending application is more generic with regard to the type of gene therapy vector that encodes Kir7.1, and ii) the instant claims require particular vector elements (including ITRs, PRE, and polyadenylation signal), as well as constructs, cells and virus particles, which are not present in the copending claims. However, as described above in the rejections under 35 U.S.C. §103, these elements and features are known in the prior art (see above). Thus, the instant claims were prima facie obvious to one of ordinary skill in the art in view of the copending application and Kirn, Miller, Nenoi, Mallet, Petrukhin, Miller II, Wang, as evidenced by GenBank accession: MG550105.1, and GenBank accession: MK801287.1 (supra).
In summary, Kirn teaches AAV vectors that comprise transgenes (heterologous polynucleotides) for gene therapy (paras. [0010], [0054], [0088], and [00247-0048]), wherein the heterologous polynucleotide is flanked by AAV ITRs (para. [0054]), & [0088]). Kirn further discloses that the AAV may comprise an RPE specific promoter linked to the transgene, which can be a KCNJ13 gene, which encodes Kir7.1 protein (paras. [0224] & [0217]). Additionally, Kirn’s compositions encompass rAAV virions (viral particles), which include an rAAV polynucleotides, as well as polynucleotides encoding rAAV, such as plasmids (para. [0053]). Kirn also discloses host cells useful for producing rAAV, which can be stably genetically modified with a nucleic acid or transiently genetically modified with a nucleic acid (para. [0231]). Furthermore, Kirn teaches that helper virus functions, which allow AAV replication and packaging, may be provided in a number of ways, including by providing helper virus or polynucleotide sequences encoding the requisite functions to a producer cell in trans, by a plasmid or other expression vector (para. [0057]). Kirn also provides a pharmaceutical composition comprising rAAV and a pharmaceutically acceptable carrier, diluent, excipient, or buffer suitable for use in a human or non-human patient (para. [0232]).
Miller teaches viral vectors comprising a KCNJ13 gene that is 99% identical in sequence to SEQ ID NO: 25 (see Appendix A: alignment of the instant SEQ ID NO: 25 with Miller’s SEQ ID NO: 1; Miller, Table 1, Abstract, generally, paras. [0022], [0057], [0091]). Miller further teaches that its compositions may be used for modulation of the gene activity in vivo for prophylactic and therapeutic purposes (Abstract).
Nenoi teaches AAV gene therapy vectors comprising a 5’ ITR that is 100% identical in sequence to SEQ ID NO: 23, a therapeutic gene sequence, a polyadenylation sequence, and a 3’ ITR that is 100% identical in sequence to SEQ ID NO: 28 (paras. [0009] & [0039-0041]; 5’ ITR and 3’ITR sequences labeled as “SEQ ID NO: 4” and “SEQ ID NO: 5” in Nenoi, respectively).
Mallet teaches vectors, compositions, and methods for delivering transgenes into mammalian cells (Abstract). Mallet further discloses that of various tested elements and sequences from eukaryotic mRNAs that could enhance transgene expression in mammalian cells, WPRE gave the highest level of expression (paras. [0022-0026]). Additionally, Mallet discloses the WPRE element sequence, SEQ ID NO: 1, which from nucleotides 7-604 is 100% identical to the instant SEQ ID NO: 26 (Mallet SEQ ID NO: 1). Mallet further discloses that the vectors may be plasmids, recombinant viruses, or specifically AAVs (para. [0038]). Further, Mallet discloses that its compositions and methods may be used in epithelial cells and other tissues, organs, or cell types (para. [0048]).
Petrukhin teaches human and mouse DNA sequences that encode the gene CG1CE, which, when mutated, is responsible for Best’s macular dystrophy (Abstract). Petrukhin further discloses that Best’s macular dystrophy is also known as hereditary macular dystrophy or Best’s vitelliform macular dystrophy (VMD2; para. [0005]). Petrukhin also discloses a human genomic CG1CE DNA that has the nucleotide sequence SEQ ID NO: 1, which is localized to the RPE, which has a fragment with 100% sequence identity to the instant SEQ ID NO: 24 (nts 4582-5557, paras. [0020,0119-0120]).
Miller II teaches AAV vectors for human gene therapy, wherein vectors include a selectable bacterial marker and replication origin, and specifically the AAV shuttle vector AAV2-TOA, which contains a bacterial replication origin and antibiotic resistance genes (p. 11436, col. 2; Abstract; p. 11439, para. 1). Miller II discloses that such plasmid DNAs from bacteria may be used for AAV vector production (p. 11435, para. 2).
Wang teaches AAV-based gene therapy vectors (Abstract), that can accommodate a transcriptional cassette including promoter and polyadenylation signal (p. 668, col. 1, para. 3). Wang further discloses that Bovine growth hormone (BGH) polyadenylation signal was the strongest of various polyadenylation signals tested (Fig. 2). GenBank accession: MG550105.1 (1/10/2018) provides evidence that the nucleotide sequence of BGH is 100% identical to SEQ ID NO: 27.
GenBank accession: MK801287.1 teaches an AAV cloning vector that possesses vector backbone, a replication origins, and an ampicillin resistance gene that is 99.8% identical (2592 of 2597 nucleotides) in sequence to the corresponding vector sequence features in SEQ ID NO: 22.
Thus, each limitation of the instant claims is rendered obvious by the copending application in view of the combined teachings of Kirn, Miller, Nenoi, Mallet, Petrukhin, Miller II, Wang, as evidenced by GenBank accession: MG550105.1, and GenBank accession: MK801287.1 (see rejections under 35 U.S.C. §103 above for further claimed sequence information).
This is a provisional nonstatutory double patenting rejection.
Conclusion
No claim is allowed. Any inquiry concerning this communication or earlier communications from the examiner should be directed to JEFFREY MARK SIFFORD whose telephone number is (571)272-7289. The examiner can normally be reached 8:30 a.m. - 5:30 p.m. ET with alternating Fridays off.
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/JEFFREY MARK SIFFORD/Examiner, Art Unit 1671
/JANET L ANDRES/Supervisory Patent Examiner, Art Unit 1671